At what dose does ALD-52 produce psychosis?

Effects like psychosis are typically reported at common doses and above. A common oral dose of ALD-52 is 100–175 µg.

What other substances cause psychosis?

Other substances documented to produce psychosis include 1P-ETH-LAD, Methamphetamine, 3,4-CTMP, 1P-LSD, Myristicin, and 35 more.

Psychosis from ALD-52 — Detailed Guide

Q: Does ALD-52 cause psychosis?

Yes. Psychosis is a documented cognitive effect of ALD-52. Psychosis is a serious psychiatric state involving a fundamental break from consensus reality — characterized by firmly held false beliefs (delusions), perception of things that are not there (hallucinations), disorganized thought and speech, and a loss of the ability to distinguish internal mental events from external reality.

Psychosis from ALD-52

cognitivePsychedelic

Psychosis + ALD-52

Effect category

cognitive

Substance class

Psychedelic

Chemical class

Lysergamides

Routes of administration

oral

Other effects from ALD-52

Other substances causing this effect

Psychosis + ALD-52

Effect category

cognitive

Substance class

Psychedelic

Chemical class

Lysergamides

Routes of administration

oral

Other ALD-52 effects

Substances causing psychosis

ALD-52 is known to produce psychosis, a cognitive effect. Psychosis is a serious psychiatric state involving a fundamental break from consensus reality — characterized by firmly held false beliefs (delusions), perception of things that are not there (hallucinations), disorganized thought and speech, and a loss of the ability to distinguish internal mental events from external reality.

About Psychosis

Psychosis represents one of the most severe adverse cognitive outcomes associated with psychoactive substance use. It is not a single symptom but a syndrome — a constellation of related disruptions to perception, belief, and thought that collectively produce a state in which the person has lost meaningful contact with shared reality. The defining features include delusions (fixed false beliefs maintained with absolute conviction),hallucinations (perceiving things that are not present, across any sensory modality),thought disorder (disorganized, incoherent, or tangential thinking and speech), andloss of insight (the inability to recognize that one's perceptions and beliefs are abnormal).

What distinguishes psychosis from the altered perceptions produced by a "normal" psychedelic or dissociative experience is fundamentally about insight. A person having a psychedelic trip may see geometric patterns overlay their visual field, but they know they have taken a substance and that the patterns are drug-induced. A person experiencing psychosis may see the same patterns but believe they represent coded messages from a government surveillance network — and no amount of rational argument can shake this conviction. The loss of the ability to reality-test one's own perceptions is the critical threshold that separates an altered state from a psychotic one.

Substance-induced psychosis can arise through several pathways. Acute intoxication psychosis can occur with high doses of psychedelics, stimulants, cannabis, and deliriants — the sheer intensity of the altered state overwhelms the person's capacity to maintain orientation.Stimulant psychosis is particularly well-documented: extended use of amphetamines, methamphetamine, or cocaine, especially combined with sleep deprivation, can produce a paranoid psychotic state that closely resembles acute schizophrenia, complete with persecutory delusions, auditory hallucinations, and disorganized behavior.Cannabis-induced psychosis can occur in predisposed individuals, sometimes after a single heavy exposure.Withdrawal psychosis can accompany withdrawal from alcohol and benzodiazepines.

The relationship between substance use and psychosis is bidirectional and complex. Substances can trigger psychotic episodes in individuals with latent vulnerability (genetic predisposition to schizophrenia-spectrum disorders), can worsen existing psychotic conditions, and can produce transient psychotic states in individuals with no underlying vulnerability. Cannabis use during adolescence has been identified as a significant risk factor for the later development of psychotic disorders, with a dose-response relationship. However, most people who use these substances never experience psychosis, and the interaction between substance exposure and individual vulnerability is not well enough understood to predict individual risk.

Harm reduction note: Psychosis is a psychiatric emergency. If someone has lost contact with reality — believing things that are clearly not true, acting on hallucinated perceptions, unable to recognize that they are intoxicated — they need professional help. Do not attempt to argue them out of delusions, as this typically escalates agitation. Ensure physical safety, speak calmly and simply, and call for medical assistance. Individuals with a personal or family history of psychotic disorders should exercise extreme caution with all psychoactive substances, particularly cannabis, psychedelics, and stimulants.

How ALD-52 Produces This Effect

ALD-52 through its metabolite LSD acts as a partial agonist at most serotonin receptor subtypes, including the 5-HT1A, 5-HT2A, 5-HT2B, 5-HT2C and 5-HT6 receptors. It can also be expected to act as an agonist at dopamine receptors such as D2. The psychedelic effects are believed to come from ALD-52's efficacy at the 5-HT2A, 5-HT2C, and 5-HT1A receptor subtypes.

ALD-52, alongside 1P-LSD and 1B-LSD, act as prodrugs for LSD, though it is unclear as to whether it is capable of exerting its own effects as a parent substance. It has been found that ALD-52 metabolizes into two distinct metabolites, N-deethyl ALD-52 and N6-demethyl ALD-52 (nor-ALD-52) in addition to its' primary metabolite LSD. ALD-52 is metabolized by CYP3A4 which does the N6-deallylation. Additionally, CYP2D6 is involved in the hydroxylation process. and this may extend to A and this may extend to ALD-52.

The toxicity and long-term health effects of recreational ALD-52toxic dose is unknown. This is because ALD-52 is a research chemical with a very limited history of human use.

Anecdotal evidence from people within the community who have tried ALD-52 suggests that there are no negative health effects attributed to simply trying the drug by itself at low to moderate doses and using it very sparingly (although nothing can be completely guaranteed). Independent research should always be conducted to ensure that a combination of two or more substances is safe before consumption.

As with other psychedelic substances, there are relatively few physical side effects that have been reported associated with acute ALD-52 exposure. Although no formal studies have been conducted, it is likely that as with LSD itself, ALD-52 is able to be considered non-addictive,extremely low toxicity relative to dose. It is also likely that as with LSD, there are little to no negative physical, cognitive, psychiatric or other toxic consequences associated with acute ALD-52 exposure.

However, as with LSD and psychedelics in general, it is possible that ALD-52 can act as a potential trigger for those with underlying psychiatric conditions. It is advised to be extremely cautious if it is known that a family member has bipolar disorder or schizoaffective disorder as those with a personal or family history of mental illness are generally advised not to use this substance, particularly outside of a supervised medical setting.

It is strongly recommended that one uses harm reduction practices when using this substance.

Although no formal studies have been conducted, it is not unreasonable to assume that like LSD itself, ALD-52not habit-forming and that the desire to use it can actually decrease with use.

Tolerance to the effects of ALD-52almost immediately after ingestion. After that,5-714 days to be back at baseline (in the absence of further consumption). ALD-52 presents cross-tolerance with Cross-all psychedelics, meaning that after the use of ALD-52 all psychedelics will have a reduced effect.

Overdose

The LD50 of ALD-52 is unknown. Adverse psychological reactions are common especially at higher doses. Some of these include anxiety, delusions, panic attacks and more rarely seizures. Medical attention is usually only needed if suspected of severe psychotic episodes or “fake acid” (such as 25i-NBOMe or DOB). Administration of benzodiazepines or antipsychotics may help to relieve the negative cognitive effects.

ALD-52 is currently a gray area compound within many parts of the world. This means that it is not known to be specifically illegal within most countries, but people may still be charged for its possession under certain circumstances such as under analog laws and with the intent to sell or consume.

Austria: ALD-52 is technically not illegal but it may fall in the NPSG (Neue-Psychoaktive-Substanzen-Gesetz Österreich) as an analogue of LSD.
Denmark: ALD-52 is not listed as an illegal substance in Denmark, and its chemical class 'lysergamide' is not banned under the Analogue Act (Some LSD analogues are, however, prohibited).
Germany: ALD-52 is controlled under the NpSG (New Psychoactive Substances Act) as of July 18, 2019. Production and import with the aim to place it on the market, administration to another person and trading is punishable. Possession is illegal but not penalized.
Latvia: ALD-52 is illegal in Latvia. Although it isn't officially scheduled, it is controlled as an LSD structural analog due to an amendment made on June 1, 2015.
Poland: ALD-52 is a NPS class drug in Poland, making it illegal to possess or distribute.
Singapore: ALD-52 is a Class A controlled substance.
Switzerland: ALD-52 is a controlled substance specifically named under Verzeichnis E.
United Kingdom: As of January 7, 2015, ALD-52 is specifically named in the U.K. Misuse of Drugs Act as a Class A controlled substance..
United States: ALD-52 is unscheduled in the United States. It may be considered an analogue of LSD, a Schedule I controlled substance under the Controlled Substances Act. As such, the sale for human consumption or the use for illicit non-medical or scientific research could be prosecuted as crimes under the Federal Analogue Act.
Responsible use
Research chemical
Psychedelic
Lysergamide
LSD
1P-LSD
AL-LAD
ALD-52 (Wikipedia)
ALD-52 (Erowid Vault)
ALD-52 (TiHKAL / Isomer Design)
Discussion
The ALD-52 Thread (Bluelight)
Nichols, D. E. (2016). Psychedelics. Pharmacological Reviews, 68(2), 264-355. https://doi.org/10.1124/pr.115.011478
Passie, T., Halpern, J. H., Stichtenoth, D. O., Emrich, H. M., & Hintzen, A. (2008). The Pharmacology of Lysergic Acid Diethylamide: A Review, 14, 295–314. https://doi.org/10.1111/j.1755-5949.2008.00059.x
Carhart-Harris, R. L., Muthukumaraswamy, S., Roseman, L., Kaelen, M., Droog, W., Murphy, K., … Nutt, D. J. (2016). Neural correlates of the LSD experience revealed by multimodal neuroimaging. Proceedings of the National Academy of Sciences. https://doi.org/10.1073/pnas.1518377113

ALD-52 can be administered via oral. The route of administration can influence both the onset and intensity of psychosis.

Psychosis from ALD-52

Psychosis + ALD-52

Psychosis + ALD-52

About Psychosis

How ALD-52 Produces This Effect

Dosage Context

oral

Other Substances That Cause Psychosis (40)

Cannabinoid

Deliriant

Depressant

Dissociatives

Dissociatives, Psychedelic

Entactogen, Stimulants

Essential nutrient, Neurotransmitter cofactor

Neurotransmitter

Psychedelic

Stimulants

See Also

Frequently Asked Questions

Psychosis from ALD-52

Psychosis + ALD-52

Psychosis + ALD-52

About Psychosis

How ALD-52 Produces This Effect

Dosage Context

oral

Other Effects from ALD-52 (70)

Other Substances That Cause Psychosis (40)

Cannabinoid

Deliriant

Depressant

Dissociatives

Dissociatives, Psychedelic

Entactogen, Stimulants

Essential nutrient, Neurotransmitter cofactor

Neurotransmitter

Psychedelic

Stimulants

See Also

Frequently Asked Questions